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. 2022 Jun 27;33(11):451–462. doi: 10.1097/WNR.0000000000001803

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Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Fig. 4 — Involvement of the Nrf2/HO-1 signaling pathway in the NGR1-induced inhibition of oxidative stress after SCI. (a–c) Quantitative analysis of MDA, SOD, GSH-PX in the Sham + vehicle, SCI + vehicle, SCI + NGR1, and SCI + NGR1 + ML385 groups at 14 days after SCI. N = 5. Data are represented as mean ± SEM. One-way analysis of ANOVA with Turkey’s post hoc tests was used. *P < 0.05 vs. the Sham + vehicle group; ^#P < 0.05 vs. the SCI + vehicle group; ^&P < 0.05 vs. the SCI + NGR1 group. ANOVA, analysis of variance; GSH-PX, glutathione peroxidase activity; HO-1, heme oxygenase-1; MDA, malonaldehyde; NGR1, notoginsenoside R1; Nrf2, nuclear factor erythroid 2 related factor 2; SCI, spinal cord injury; SOD, superoxide dismutase.